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Platelet‐derived growth factor‐BB phosphorylates heat shock protein 27 in cardiac myocytes
Author(s) -
Takenaka Motoki,
Matsuno Hiroyuki,
Ishisaki Akira,
Nakajima Keiichi,
Hirade Kouseki,
Takei Mariko,
Yasuda Eisuke,
Akamatsu Shigeru,
Yoshimi Naoki,
Kato Kanefusa,
Kozawa Osamu
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10717
Subject(s) - hsp27 , platelet derived growth factor receptor , p38 mitogen activated protein kinases , phosphorylation , mitogen activated protein kinase kinase , protein kinase a , microbiology and biotechnology , ask1 , map kinase kinase kinase , mitogen activated protein kinase , map2k7 , kinase , cyclin dependent kinase 2 , biology , heat shock protein , growth factor , biochemistry , hsp70 , receptor , gene
Abstract It is recognized that heat shock protein 27 (HSP27) is highly expressed in heart. In the present study, we investigated whether platelet‐derived growth factor (PDGF) phosphorylates HSP27 in mouse myocytes, and the mechanism underlying the HSP27 phosphorylation. Administration of PDGF‐BB induced the phosphorylation of HSP27 at Ser‐15 and ‐85 in mouse cardiac muscle in vivo. In primary cultured myocytes, PDGF‐BB time dependently phosphorylated HSP27 at Ser‐15 and ‐85. PDGF‐BB stimulated the phosphorylation of p44/p42 mitogen‐activated protein (MAP) kinase, p38 MAP kinase, and stress‐activated protein kinase/c‐Jun N‐terminal kinase (SAPK/JNK) among the MAP kinase superfamily. SB203580, a specific inhibitor of p38 MAP kinase, reduced the PDGF‐BB‐stimulated phosphorylation of HSP27 at both Ser‐15 and ‐85, and phosphorylation of p38 MAP kinase. However, PD98059, a specific inhibitor of MEK, or SP600125, a specific inhibitor of SAPK/JNK, failed to affect the HSP27 phosphorylation. These results strongly suggest that PDGF‐BB phosphorylates HSP27 at Ser‐15 and ‐85 via p38 MAP kinase in cardiac myocytes. © 2003 Wiley‐Liss, Inc.